ELECTROPHYSIOLOGICAL CHARACTERIZATION OF SPINAL NEURONAL RESPONSE PROPERTIES IN ANESTHETIZED RATS AFTER LIGATION OF SPINAL NERVES L5-L6

1. Despite a number of models of nerve injury, few studies have examin ed how peripheral nerve injury influences spinal somatosensory process ing. 2. Ligation of two (L5-L6) of the three spinal nerves that form t he sciatic nerve produces a partial denervation of the hindlimb. Follo wing ligation, rats exhibited withdrawal responses to normally innocuo us punctate mechanical and cooling stimuli (acetone) applied to the le sioned hindpaw. Such mechanical and cooling allodynia was not observed in sham-operated rats. 3. A significantly greater proportion of spina l neurones of ligated rats exhibited spontaneous activity at post-oper ative (PO) days 7-10 (P = 0.03) and 14-17 (P = 0.0001), compared with sham controls. The frequency of the spontaneous activity was significa ntly higher than that of the sham controls (P = 0.03 and P = 0.02 for days 7-10 and days 14-17, respectively). 4. At the earlier PO period, significantly (P = 0.02) more neurones of spinal nerve-ligated (SNL) r ats responded to brush compared with the sham controls; at the later P O period the proportion of neurones of SNL rats responsive to prod was significantly (P = 0.007) reduced compared with the sham controls. Th e magnitude of the evoked neuronal response of SNL rats at PO days 7-1 0 was comparable to that of the sham controls. The magnitudes of brush - and prod-evoked neuronal responses of SNL rats were significantly sm aller (P = 0.05 and P = 0.002, respectively) than the sham controls at PO days 14-17. In addition, neuronal responses of SNL rats to mechani cal punctate stimuli and the C fibre-evoked neuronal responses were si gnificantly reduced at the later PO period, compared with sham control s. A beta-fibre-induced wind-up was not observed under any conditions. 5. These complex changes in neuronal responses are both time and moda lity dependent. The plasticity of some of the neuronal and behavioural responses following nerve injury was difficult to reconcile. We sugge st that an interplay between pathological peripheral and central mecha nisms may account for some of the changes that could contribute to all odynia and hyperalgesia.